Furosemide-sensitive calcium rise induced by GABAA-receptor stimulation in cultures of embryonic rat striatal neurons.

Changes in [Ca2+]i induced by gamma-aminobutyric acid (GABA) were investigated in primary cultured neurons obtained from fetal rat striatum. GABA and muscimol induced [Ca2+]i rise, and bicuculline blocked the effect of GABA. The [Ca2+]i elevating effect of GABA was also abolished by removal of extracellular Ca2+ or by application of nicardipine. Furthermore, furosemide, an inhibitor of Na+/K+/ 2Cl- co-transport, reversibly inhibited the GABA-induced [Ca2+]i rise. These results suggest that due to the elevated level of intracellular Cl- maintained by Na+/K+/2Cl- transport activity in these neurons, opening of GABAA-receptor-associated Cl- channels results in Cl- efflux, leading to membrane depolarization and activation of L-type voltage-dependent Ca2+ channels.